Introduction
BACKGROUND:
Previous population based studies including both the Global allergy &
Asthma European (GA2LEN) survey1 and
Canadian National Population Health survey2 suggest a
strong association between CRS prevalence and active
smoking,
with a possible dose dependent association in the
GA2LEN1 study finding a 1.5%
increase in prevalence for each year smoked. Several national and
international studies have also looked at smoking and its relationship
to chronic rhinosinusitis (CRS); with eleven out of thirteen studies in
a recent systematic review reporting increased CRS prevalence in
smokers.3 Conversely a small number of studies4,5 have reported a lack of any strong association and
some previous epidemiological studies have the potential to overestimate
disease prevalence on methodological
design.
The
2000 National (England and Wales) Sino-Nasal Audit identified that
around 20% of patients with CRS/ nasal polyps regarded themselves as
active smokers, compared to a national adult smoking rate at the time of
27%.6
A number of studies have examined the possible effects of smoking on the
sinonasal mucosa with variable results. This lack of consensus may
result from a lack of standardisation but also highlights that a
combination of different pathophysiological mechanisms may co-exist.
Chistenson et al3 summarised prominent findings from
available invitro and invivo studies. In vitro studies have suggested a
number of possible mechanisms with smoking causing alterations in
chloride ion transport,7, 8 reduced mucociliary
clearance8 and or reduced ciliary
generation.9 In vivo results are also conflicting with
possible changes in histology,10 mucociliary
transport11 and inflammatory
cytokines12 underlying disease development. The
aetiological role of the sinonasal microbiome is another topical area
where there has been increasing research with respect to smoking and its
potential roles in altering this microbiome and or encouraging biofilm
formation.13Some
in vitro experiments have shown that repetitive exposure of tobacco
smoke can promote biofilm formation within bacterial isolates from CRS
patients,14however any underlying mechanism remains poorly understood. In contrast
Zhang et al15 failed to find any difference between
smoking status and biofilm formation within sinus cultures taken at the
time of endoscopic surgery.
With such heterogeneity in existing research no strong conclusions can
currently be drawn on the exact pathophysiological mechanisms involved
in CRS. Understanding the relationship of smoking to the health of
sinonasal mucosa is however an important step to help direct patient
care and education and may allow more accurate discussion on the likely
clinical outcomes of any subsequent therapy and surgical intervention.
The Chronic Rhinosinusitis Epidemiology Study (CRES) was a prospective,
questionnaire-based, case-control study conducted between October 2007
and September 2013 at thirty tertiary/secondary care sites across the
United Kingdom. Patients with diagnosed CRS alongside healthy control
subjects were asked to complete a single, study-specific questionnaire,
capturing a variety of demographic and socio-economic variables,
environmental exposures and medical co-morbidities (See appendix 1).
CRES was designed to distinguish differences in socio-economic status,
geography, medical/psychiatric co-morbidity, lifestyle and overall
quality of life between patients with CRS and healthy controls. The
specific aim of this analysis of the CRES database was to determine
whether active smoking represents a risk factor for CRS development and/
or whether smokers experience an increased symptom burden than
non-smokers. Understanding causal links will allow for more informed
decision making and may clarify the potential role of smoking cessation
in CRS symptom control.